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            <h1 class="art-title">Latest Articles</h1>
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                <span class="label openaccess">Open Access</span>
                <span class="label articletype">Review</span>
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                <a href="http://www.cancercellresearch.org/PDF/20192201.pdf" class="artical-title">Clinical Diagnosis and Treatment of Retroperitoneal Primitive Neuroectodermal Tumors</a>
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              <div class="artical-author">by
                <a href="#" class="author-link"><span class="author">Xiangyang He</span></a>
                <a href="#" class="author-link"><span class="author">Lichao Cha</span></a>
                <a href="#" class="author-link"><span class="author">Guorui Li</span></a>
                <a href="#" class="author-link"><span class="author">Qian Wei</span></a>
                <a href="#" class="author-link"><span class="author">Fabo Qiu</span></a>
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                <div class="abstract-full inline">
                  To investigate characteristics of diagnosis and treatment of retroperitoneal primitive neuroectodermal tumors. The clinical data of 8 patients with retroperitoneal primitive neuroectodermal tumors admitted to the Affiliated Hospital of Qingdao University from May 2011 to September 2017 were retrospectively analyzed. All patients were confirmed by pathology as primitive neuroectodermal tumors. 2 cases underwent needle biopsy before surgery, 3 cases were given palliative resection, 5 cases accepted complete resection of the tumor, and 4 cases were combined organ resection. The retroperitoneal primitive neuroectodermal tumor is a highly malignancy and is difficult to diagnose before operation. The main treatment is surgery-based comprehensive treatment, and the prognosis of this disease is poor.
                <a href="http://www.cancercellresearch.org/PDF/20192201.pdf">Full article</a></div>
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                <span class="label openaccess">Open Access</span>
                <span class="label articletype">Review</span>
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                <a href="http://www.cancercellresearch.org/PDF/20192202.pdf" class="artical-title">Protective effects of hydroxysafflor yellow an on high oxidized low density lipoprotein induced human coronary artery endothelial cells injuries</a>
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              <div class="artical-author">by
                <a href="#" class="author-link"><span class="author">Tianjie Miao</span></a>
                <a href="#" class="author-link"><span class="author">Lei Qian</span></a>
                <a href="#" class="author-link"><span class="author">Fei Yu</span></a>
                <a href="#" class="author-link"><span class="author">Longgang Hu</span></a>
                <a href="#" class="author-link"><span class="author"> Han Jiaqi</span></a>
                <a href="#" class="author-link"><span class="author"> Yi An</span></a>
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                <div class="abstract-full inline">
                  The aim of this study was to investigate the injury of human coronary artery endothelial cells (HCAECs) induced by high oxidized low density lipoprotein (ox-LDL) and to examine the protective effect of hydroxysafflor yellow A (HSYA) on HCAECs injury. It was found that in the high ox-LDL group the content of NO, the expression of endothelial nitric oxide synthase (eNOS) mRNA and protein were decreased. The expression of LDH, lectin-like low-density lipoprotein receptor 1 (LOX-1) mRNA and LOX-1 protein were up-regulated. The number of apoptotic cells were significantly increased after deal with high ox-LDL compared with the control group. Furthermore, in the high ox-LDL+HSYA group, the cell survival rate, the release of NO and the expression of eNOS mRNA and eNOS protein were increased. The secretion of LDH and the expression of LOX-1 at the level of mRNA and protein were down-regulated. The number of apoptosis were significantly reduced after combined with HSYA compared with the high ox-LDL group. Therefore, high ox-LDL had an obvious damage to HCAECs. The HSYA inhibited the high ox-LDL-induced HCAECs injury and protected and promoted the cell repaired, possibly by up-regulating the eNOS gene and protein expression, increasing NO release, inhibiting LDH release and down-regulating LOX-1 mRNA and protein expression to achieve the effect. The treatment and secondary prevention of coronary heart disease, as well as the recovery of patients undergoing postoperative percutaneous coronary intervention (PCI), will benefit to a large extent.
                <a href="http://www.cancercellresearch.org/PDF/20192202.pdf">Full article</a></div>
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                <span class="label openaccess">Open Access</span>
                <span class="label articletype">Review</span>
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                <a href="http://www.cancercellresearch.org/PDF/20192203.pdf" class="artical-title">The study of correlation between EB virus with Chronic lymphoblastic leukemia</a>
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              <div class="artical-author">by
                <a href="#" class="author-link"><span class="author">Changkai Zhang</span></a>
                <a href="#" class="author-link"><span class="author">Wei Lu</span></a>
                <a href="#" class="author-link"><span class="author">Xiaofang Guo</span></a>
                <a href="#" class="author-link"><span class="author">Hongzai Guan</span></a>
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              <div class="summary-content">
                <div class="abstract-full inline">
                  To investigate the relationship between EBV infection and the occurrence and development of chronic lymphoblastic leukemia (CLL), and to provide a reliable basis for revealing the close relationship between EBV infection and CLL. Fluorescence quantitative polymerase chain reaction (FQ-PCR) was used to detect the copy numbers of EBV-DNA from the bone marrow of 80 CLL patients. 40 healthy persons were control group and 40 cases for clinical follow-up. The results showed that the EBV positive rates (EBV+) of CLL patients and healthy controls were 25% (20/80) and 7.5% (3/40) respectively. Chromosome analysis showed that the rate of EBV+ in CLL patients with chromosome abnormalities was 18.75% (3/16), while the rate of EBV- was 81.25% (13/16), and no significant difference was observed between chromosome abnormality and EBV infection (2=0.21, p>0.05). Clinical follow-up showed that the relapse rate mortality rate of EBV+ and EBV- groups within 5 years were 55.6% (10/18), 28.6% (12/42) and 44.4% (8/18), 4.7% (2/42), respectively
                <a href="http://www.cancercellresearch.org/PDF/20192203.pdf">Full article</a></div>
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                <span class="label openaccess">Open Access</span>
                <span class="label articletype">Review</span>
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                <a href="http://www.cancercellresearch.org/PDF/20192204.pdf" class="artical-title">Greig cephalopolysyndactyly syndrome caused by novel GLI3 mutation: a family report</a>
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              <div class="artical-author">by
                <a href="#" class="author-link"><span class="author">Ying Tang</span></a>
                <a href="#" class="author-link"><span class="author">Juan Ge</span></a>
                <a href="#" class="author-link"><span class="author">Tang Li</span></a>
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              <div class="summary-content">
                <div class="abstract-full inline">
                  To investigate the clinical feature and gene mutaiton of Greig cephalopolysyndactyly syndrome (GCPS). The clinical data and the whole exome sequencing results of two patients with GCPS in the same family were retrospectively analyzed. The related literatures were reviewed. The propositus was a 7-month-old girl who manifested a prominent forehead and widely spaced eyes, but have no evident growth developmental retardation. Her mother, 25-year-old, manifested a prominent forehead, macrocephaly, hypertelorism, broad thumbs and halluces in both hands and feet, and scoliosis. A novel missense mutation in GLI3 gene was found by whole exon sequencing of the proband, which caused the 478th amino acid of the GLI3 gene encoded protein which changed from tyrosine to cysteine acid. The GLI3 mutation was identified in his mother by Sanger sequencing. Her father GLI3 gene was normal. The same missense mutation was not retrieved in the HGMD. Reports of the mutation were not found in the previous research. It may be a new mutation. The GCPS is a pleiotropic, multiple congenital anomaly syndrome caused by GLI3 gene mutation or deletion. More than 70 GLI3 gene mutation sites with GCPS had been reported and the most common type was frame shift mutations. Awareness by clinicians of the array of phenotypes manifest in GCPS and gene detection will aid in clinical diagnosis.
                <a href="http://www.cancercellresearch.org/PDF/20192204.pdf">Full article</a></div>
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